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No variants that fulfilled the criteria to be likely pathogenic or pathogenic according to the American College of Medical Genetics and Genomics (ACMG) that could explain a metabolic disorder with an autosomal recessive inheritance were identified [22]
CSE is activated by phosphorylation by AKT and expression is upregulated by farnesoid X receptor (FXR) and specificity protein 1 (Sp1) [39]
Although no randomized trials exist, the uniformity of observational data has led GeneReviews and European neurometabolic taskforces to issue class I recommendations for immediate high-dose riboflavin upon molecular diagnosis (14)
